Key Points from Prof. Thomas Borody’s 2008 Interview on MAP and Crohn’s

Virus MicrographMany of you may have already watched Prof. Thomas Borody’s nine part video series in which he discusses the role of Mycobacterium avium subsp. paratuberculosis (MAP) in Crohn’s disease and answers a myriad of questions. The series, which is about 90 minutes, is still relevant today, though some information may be outdated. For those who don’t have the time to watch it in its entirety, we’ve done our best to summarize some of the key points. We’d encourage you to see for yourself what Prof. Borody has to say, and why his approach is resulting in a much higher rate of remission than any other Crohn’s disease therapy. Sign up for our newsfeed to get the first look at new articles like this one!

  • MAP is present in the environment. It’s in dairy, beef and water, so it’s impossible to avoid exposure unless one were to live in a bubble.
  • The MAP bacteria passes from mother to baby via breast milk.
  • As long as Crohn’s disease patients stay on Anti-MAP antibiotic therapy (AMAT), there is no need to restrict the diet.
  • All of the patients in one study, who were successfully in remission on AMAT therapy, relapsed at some point once they stopped AMAT. Sometimes it took years, but eventually they all relapsed.
  • Pulsing (going on and off) AMAT could create resistant strains of MAP.
  • Koch’s postulates have been proven for MAP’s causation of Crohn’s disease. (Koch’s postulates are the standard four principles used for determining that a particular organism causes a specific disease.)
  • The proof of MAP’s role in Crohn’s disease in many doctor’s minds is not the research or Koch’s postulates, but rather the approval of the FDA of a treatment, which only approves the safety and efficacy of the therapy.
  • When treating patients with a triple antibiotic combination pill, Prof. Borody gradually increases the dosage to lessen side effects. The bioavailability (absorption) of the drugs are actually greater when taken together, possibly due to a carrier added to the pill.
  • For those who do not respond to AMAT, it may be a different bug or a complicating condition that is causing their Crohn’s disease.
  • A genetic predisposition which renders the immune system unable to rid the cells of intracellular infection is probably present in most Crohn’s disease patients.
  • Even the flawed Selby study (using a version of AMAT) produced the highest remission rate of any Crohn’s disease trial at 66%.
  • The detractors who argue that AMAT only changes the gut flora are incorrect. Standard antibiotics that are known to alter the gut flora don’t improve Crohn’s disease symptoms, but AMAT (which specifically targets MAP) improves Crohn’s disease symptoms.
  • Just because the researchers can’t see MAP in Crohn’s disease tissues doesn’t mean that it’s not there. This is sometimes the case in leprosy, which has a proven pathogenic agent. Detection methods for MAP are not yet advanced enough to detect MAP reliably.
  • Standard Crohn’s disease medications may suppress MAP levels enough to where it becomes undetectable.
  • The autoimmune theory of Crohn’s disease is dead.
  • The dysbiosis theory for Crohn’s disease is not valid, because if the body was reacting to bad bugs in the gut, then the tissue that touches those bugs would be damaged. However, colitis occurring in the distal area of the colon and the patchy accordion-like damage common in the small intestine of Crohn’s disease patients disproves that, since the bad bugs would touch the healthy areas as well as the diseased areas.
  • TNF-alpha is released from cells infected with MAP.
  • Remicade works by binding to cells that are producing TNF-alpha, likely due to MAP infection, and causing cell death.
  • MAP is an intracellular bacteria that is incapable of dissemination (spreading) in the body like tuberculosis.
  • In Iceland, the Crohn’s disease epidemic only began once sheep infected with MAP were introduced. Prior to that, the sheep in Iceland were not MAP infected.
  • It has been shown that the same pathogen will cause different symptoms in humans vs. animals because they are not the same species. MAP infection sometimes manifests differently in humans vs. animals for this reason.
  • There are no known non-pathogenic mycobacterial species. All mycobacteria are harmful.
  • Animals with terminal MAP disease are commonly culled and put into the human food supply.
  • MAP occurs in subhuman primates in the wild. Dogs and chickens can carry it as well.
  • Borody believes it’s less important to research genetic causes for Crohn’s disease because you can’t change genes, and genetic mutation doesn’t explain the increased rate of Crohn’s disease. It’s better to look at treatments for MAP.
  • A lot of answers are going to come from biofilms.
  • There are a large number of genetically diverse MAP species, similar to H. pylori. One patient could have multiple strains of MAP.
  • Going forward, Prof. Borody believes the key areas of research are MAP detection methods and trials of MAP specific antibiotics.

Click here to view the first part of Prof. Borody’s interview.

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